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A dose-response relation was established between prostaglandins and formation of adenosine 3',5'-monophosphate in the mouse ovary. The prostaglandin antagonist, 7-oxa-13-prostynoic acid, blocked the stimulatory effect of prostaglandin E(1), prostaglandin E(2), and luteinizing hormone on adenosine 3',5'-monophosphate formation in a competitive manner. Kinetic studies made it possible to suggest that there is a single luteinizing-hormone-related prostaglandin receptor in mouse ovaries, and that activation of this prostaglandin receptor is an essential requirement in the action of luteinizing hormone to stimulate adenosine 3',5'-monophosphate formation and steroidogenesis.

1. Resealed ghosts were prepared containing much potassium, very little sodium, and adenosine triphosphate (ATP), adenosine diphosphate (ADP) and (32)P-labelled orthophosphate (P(i)) at concentrations such that the ratio [ATP]/([ADP].[P(i)]) was low. Iodoacetate, iodoacetamide or both were also present. The ghosts were incubated in high-sodium, potassium-free media with and without ouabain, or in high-potassium media, and the incorporation of (32)P into ATP and ADP in 15 min was measured.2. There was some incorporation of (32)P into the nucleotides whatever the medium, possibly because of the residual activity of glycolytic enzymes, but in every experiment there was extra incorporation when the ghosts were in a high-sodium, potassium-free medium. This extra incorporation was largely abolished by ouabain (5 experiments) and partly abolished by oligomycin (1 experiment).3. It seems that if conditions are such that the over-all reaction associated with transport ATPase activity leads to an increase in free energy, the transport system will run backwards at a measurable rate and ATP will be synthesized at the expense of energy derived from ionic concentration gradients.4. The nature of the transport system is discussed in the light of the findings of this paper and the four preceding papers.

Adenyl cyclase activity in the pineal gland of rats was determined by measuring the rate of formation of radioactive cyclic 3',5'-adenosine monophosphate from (14)C-labeled adenosine triphosphate. Norepinephrine added in vitro to pineal homogenates enhanced this activity, while denervation of the pineal gland by superior cervical ganglionectomy did not significantly reduce it. The enzyme in these denervated glands was more responsive to the stimulatory effects of norepinephrine.

Aerobacter cloacae UW-C83 and Escherichia coli K-12 were grown under various anaerobic environments. Y(atp) values were calculated by determination of cell weights and analyses for fermentation products. These Y(atp) values are compared with others reported in the literature. Limitation of growth by factors other than adenosine triphosphate supply is discussed.

1. The activities of NMN adenylyltransferase and an enzyme that synthesizes poly (ADP-ribose) from NAD were investigated in the various classes of rat liver nuclei fractionated by zonal centrifugation. 2. The highest specific activities of these two nuclear enzymes occur in different classes of nuclei. In very young and in mature rats it was shown that a correlation exists between DNA synthesis and NMN adenylyltransferase activity, but in rats of intermediate age this correlation is less evident. The highest activities of the enzyme that catalyses formation of poly (ADP-ribose) are in the nuclei involved in the synthesis of RNA. 3. The significance of these results in relation to NAD metabolism is discussed.

Experiments are reported which throw new light on the problem of ammonia production by muscle and, probably, by other tissues.

Thyrocalcitonin (TCT) increased the rate of accumulation of adenosine 3':5'-cyclic phosphate (cyclic AMP) when added to incubations containing washed particles from whole rat kidney, adenosine triphosphate (ATP), MgSO(4), and caffeine. The maximum stimulatory effect of TCT, 44 +/- 6.7 per cent, was always less than the 150 to 250 per cent increase produced by parathyroid hormone (PTH). The effect of both hormones together was no greater than that of PTH alone when each was present at a maximally effective concentration. Since neither TCT nor PTH altered the rate of degradation of cyclic AMP by the kidney preparation, it may be inferred that their effects on cyclic AMP accumulation are the result of increased formation of cyclic AMP. Adenyl cyclase activity in homogenates of renal cortex was stimulated to a greater extent by TCT and PTH than was that of medulla, whereas, as reported earlier, the effect of vasopressin was much larger with homogenates of medulla. The accumulation of cyclic AMP in incubations of rat kidney cortex slices was increased 20 to 60 per cent by TCT and 50 to 140 per cent by PTH. The accumulation of cyclic AMP in incubations of rat calvaria was increased about threefold with TCT and nine to tenfold with PTH, while reduced and alkylated TCT had less than 10 per cent of the activity of TCT. These observations are consistent with the view that the physiological effects of TCT and PTH in kidney and bone are secondary to the enhanced formation of cyclic AMP.